SUN-117 A Rare Case of Virilization in a Postmenopausal Woman with Concurrent Hypercalcemia

Abstract Disclosure: R. Pandya: None. L. Hayward: None. B. Hettinger: None. Introduction: The combination of hypercalcemia and androgen excess in postmenopausal women is rare and demands careful diagnostic evaluation. Hypercalcemia with elevated parathyroid hormone (PTH) is most commonly associated with primary hyperparathyroidism, while androgen excess typically points to an androgen-secreting tumor of ovarian or adrenal origin. This case highlights the importance of a comprehensive assessment to determine the underlying cause when both conditions coexist, including neoplastic, paraneoplastic, and genetic factors. Case Presentation: A 71-year-old postmenopausal female was referred to endocrinology for evaluation of hypercalcemia (corrected calcium: 12.3 mg/dL, normal: 8.6-10.2 mg/dL), which had been ongoing for one year, along with elevated parathyroid hormone (PTH) levels (216 pg/mL, normal: 12-88 pg/mL), raising suspicion for primary hyperparathyroidism. During the consultation, a thorough history and physical examination revealed rapid-onset hirsutism over the past 6-12 months, involving the chin, upper chest, breasts, areola, upper back, and abdomen. Additionally, she reported androgenic alopecia and mild deepening of her voice. Laboratory results revealed markedly elevated androgen levels, including total testosterone (1039 ng/dL, normal: 5-32 ng/dL), free testosterone (213.9 pg/mL, normal: 0.6-3.8 pg/mL), androstenedione (6.137 ng/mL, normal: 0.130-0.820 ng/mL), DHEA-S (248 µg/dL, normal: 9-246 µg/dL), and 17-hydroxyprogesterone (822.41 ng/dL, normal: ≤206.00 ng/dL). Imaging showed a multilobulated pelvic mass with associated ascites, raising concern for metastatic disease. Elevated CA-125 (209 U/mL, normal: <30 U/mL) further supported the suspicion of a gynecologic malignancy. Discussion: This case presents a complex clinical scenario involving the coexistence of two endocrine disorders: primary hyperparathyroidism and an androgen-secreting tumor, potentially of ovarian origin, such as Sertoli-Leydig cell tumors. Imaging of the adrenal glands did not reveal any masses, and both urine and plasma catecholamine levels were within normal limits, making adrenal tumors less likely. While the possibility of a paraneoplastic syndrome remains a consideration, we also need to keep in mind the potential for MEN1, as ovarian neuroendocrine tumors could be associated with this syndrome. Pathologic evaluation of the mass following surgical intervention will provide crucial diagnostic clarity, which will direct further management decisions. Conclusion: This case underscores the importance of a systematic approach in evaluating patients with complex presentations, especially in the context overlapping endocrine disorders. Presentation: Sunday, July 13, 2025